IADR Abstract Archives
Alveolar Bone Destruction by Autoimmune Antibodies Against Keratin-6 Peptide in Periodontitis
Objectives: The goal of this study was to investigate the role of a short sequence keratin-6 peptide (K6P) cleaved by a lysine specific cysteine proteinase in autoimmune mechanisms which may contribute to bone loss in periodontitis (PD).
Methods: K6P levels were measured in the serum of PD patients and experimental autoimmune periodontitis (EAP) using a rat model. K6P autoantibodies related to receptor activator of nuclear factor kappa-Β ligand (RANKL)-mediated osteoclast formation was determined by western blot analysis.
Results: We demonstrated overexpression of K6P in gingival keratinized, stratified squamous epithelium of PD patients. K6P expanded cell cultures were positive for T cell activation. We found a strong association between autoantibodies against K6P-induced bone resorption and osteoblast surface-bound RANKL expression in PD patients. Moreover, K6P EAP rat model demonstrated severe alveolar bone loss correlated with release of a distinct pro-inflammatory cytokine profile seen in PD.
Conclusions: Our data thus suggests that K6P autoantibodies contribute to RANKL-mediated osteoclast formation involved in pathological PD.
Methods: K6P levels were measured in the serum of PD patients and experimental autoimmune periodontitis (EAP) using a rat model. K6P autoantibodies related to receptor activator of nuclear factor kappa-Β ligand (RANKL)-mediated osteoclast formation was determined by western blot analysis.
Results: We demonstrated overexpression of K6P in gingival keratinized, stratified squamous epithelium of PD patients. K6P expanded cell cultures were positive for T cell activation. We found a strong association between autoantibodies against K6P-induced bone resorption and osteoblast surface-bound RANKL expression in PD patients. Moreover, K6P EAP rat model demonstrated severe alveolar bone loss correlated with release of a distinct pro-inflammatory cytokine profile seen in PD.
Conclusions: Our data thus suggests that K6P autoantibodies contribute to RANKL-mediated osteoclast formation involved in pathological PD.